慢性间歇性缺氧模型与气阴两虚型心脏病的相关性研究

目的考察慢性间歇性缺氧小鼠心脏形态与功能的变化,为该模型用于气阴两虚型心脏病的研究提供实验依据。方法小鼠随机分为空白对照组和模型组,空白对照组自由进食、饮水,模型组自由饮水,夜间持续禁食12 h,次日置于低压氧仓中缺氧20 min,每日1次,连续28 d。结果缺氧28 d后,模型组小鼠左心室射血分数和缩短分数明显下降;心肌细胞空泡变性,心肌细胞的线粒体水肿,肌小节散乱;心脏组织匀浆液中一氧化氮(NO),丙二醛(MDA)浓度增加,超氧化物歧化酶(SOD)活力明显下降;心肌细胞Caspase-3蛋白表达升高。结论慢性间歇性缺氧模型体现了心肌细胞损伤和心脏收缩功能减退等慢性心脏病的病理变化特点,为该模型用于气阴两虚型心脏病的研究提供了实验依据。

Correlative Study between Chronic Intermittent Hypoxia Model and Heart Disease of Qi and Yin Deficiency

Objective To observe the changes in heart morphology and function in the mice of chronic intermittent hypoxia so as to provide the experimental evidences for the study on heart disease differentiated as qi and yin deficiency. Methods The mice were randomized into a blank control group and a model group. In the blank control group,the food intake and drinking were not limited. In the model group,except for drinking,the mice were fasted at night continuously for 12 h. Since the second day,the mice were under hypoxia for 20 min in the low- pressure oxygen chamber,once every day,for 28 d. Results In 28 d of hypoxia,in the model group,the left ventricular ejection fraction and shortening fraction were reduced apparently,vacuolar degeneration of myocardial cell,mitochondria edema of myocardial cell and sarcomere scattering occurred. In heart tissue homogenate,NO and MDA concentrations were increased,SOD activity were reduced obviously,Caspase- 3 expression in myocardial cell was increased. Conclusion Chronic intermittent hypoxia model reflects the pathological characters of chronic heart disease as the injury of myocardial cell and declined heart contractile function. This model provides the experimental evidences for the study of heart disease differentiated as qi and yin deficiency.